2018 Bradycardia Clinical Guidelines

Colours correspond to Class of Recommendation.
*Atropine should not be given in patients after heart transplant.
†In patients with drug toxicity and severe symptoms, preparation for pacing should proceed simultaneously with pharmacologic treatment of drug toxicity.
AADs indicates antiarrhythmic drugs; AV, atrioventricular;BB, beta blocker; CCB, calcium channel blocker; COR, Class of Recommendation;ECG, electrocardiographic; H+P, history and physical examination; IMI, inferior myocardial infarction; IV, intravenous; PM, pacemaker; S/P, status post; and VS, vital signs.

Acute MI

  • Autonomic derangements during an acute MI are common, and small case series suggest that atropine can be used to increase heart rate. Atropine appears to be safe in those patients with atrioventricular  nodal block in the absence of infranodal  conduction system disease.
  • In contrast, it is important to recognize that the use of atropine in patients with infranodal  conduction disease or block can be associated with exacerbation of block and is potentially of harm. Aminophylline/theophylline has also been examined in this setting, and in the context of very limited data appears likely to be safe if atropine is ineffective. The methylxanthines theophylline and aminophylline (a theophylline derivative) exert positive chronotropic effects on the heart, likely mediated by inhibition of the suppressive effects of adenosine on the sinoatrial node.
  • Given that the natural course of a MI with conduction system abnormalities is frequently associated with recovery of conduction – early and unnecessary pacing should be avoided.

Heart Blocks: A Primer

  • Heart blocks can be a sign of underlying pathology such as MI, Lyme disease, myocarditis, structural heart disease, pulmonary embolism, autoimmune disease, electrolyte disturbances, medication side effects, Lenegre’s or Lev’s disease, increased vagal tone, or could be a normal variant.
  • Treatment with Atropine is indicated in bradycardic, symptomatic and/or unstable patients with a 1st or 2nd-degree Mobitz type 1 AV block. It is unlikely to be effective in high-grade blocks as the block is usually below the AV node. Atropine can still be used as a temporizing measure while setting up for transcutaneous pacing and/or transvenous pacemaker placement in high-grade blocks
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ACLS Revision: Symptomatic Bradycardia

ACLS Revision: Symptomatic Bradycardia

ATROPINE

Atropine administration should not interfere with cardiac pacing.  If there is a favorable response to atropine, the conduction abnormality is likely in the AV node. However, if the escape rhythm is originating at or below the bundle of His, there is unlikely to be a response to atropine as the more distal conducting system is not as sensitive to vagal stimulation. Response to atropine can be predicted by looking at the QRS morphology on a 12 lead ECG.  If the AV block occurs in the AV node or the Bundle of His, the escape rhythm will have a narrow QRS and will likely respond to atropine. Conversely, if the AV block occurs below the bundle of His, the escape rhythm results in a sub-junctional escape rhythm which has a wide QRS and is unlikely to respond to atropine. NOTE: Because atropine can increase cardiac demand, it is contraindicated in patients with complete heart block secondary to myocardial infarction or ischemia.

TRANSCUTANEOUS PACING

  1. Pad Placement and set up: Recommended pad placement for the best capture is anterior/posterior, as shown below. The positive pad is placed posteriorly to the left of the spine, beneath the left scapula. The negative pad is placed anteriorly between the xiphoid process and the left nipple.

Pic 2 Pad Placement

Alternatively, the pads may both be placed anteriorly, with the negative electrode placed in the V6 position and the positive electrode to the right of the sternum, under the clavicle.

Pic 3 Pad Placement

  1. Select Mode: Select the pacemaker button on the box and choose between fixed and demand modes. Fixed mode means that the pacemaker will fire at whatever rate you choose, regardless of the patient’s intrinsic rhythm. Demand mode will sense the patient’s intrinsic rhythm and pace only if needed. Most often you will start in fixed mode.
    • NOTE: If in demand mode, the leads should be placed for continuous ECG so that the pacemaker can sense the patient’s intrinsic rate to pace accordingly (double set up). This prevents the “R on T” phenomenon.
  1. Set rate and output: The initial pacing rate should be set to 60 bpm with the current set to 30 milliamperes (mA). Beware that initially, pacemaker spikes may be visualized without resultant cardiac depolarization. The current can be increased by 5-10 mA at a time until capture is seen as a definite QRS complex and T wave following each pacemaker spike (electrical capture).  Once capture is achieved, check the patient’s pulse (mechanical capture) and correlate with the pulse oximeter, blood pressure  and clinical signs (physiological capture) to ensure that a perfusing rhythm is present.  Final output should be set to 10% above threshold level to ensure continued capture. Human studies have shown that the average current necessary to achieve capture is between 65-100 mA in unstable bradycardias and about 50-70 mA in hemodynamically stable patients.

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ACLS REVISION: BRADYCARDIA…think DIE…Drugs, Ischaemia and Electrolytes

When the patient in front of you is sick, these are the three common and reversible causes of bradycardia that you need to recognize in the emergency setting that the standard ACLS trio of atropine, pacing, and adrenaline/dopamine does little or nothing to address them.